The postprandial response of adiponectin to a high-fat meal in normal and insulin-resistant subjects

Abstract

OBJECTIVE:Adiponectin is an adipose-specific protein with short-term effects in vivo on glucose and fatty acid levels. We studied the plasma concentration and the proteolytic activation status of adiponectin following the consumption of a high-fat, lowcarbohydrate meal. DESIGN: Analysis of adiponectin concentration and polypeptide structure after consumption of a fat meal. SUBJECTS: Normal subjects (n ¼ 24) and first-degree relatives of patients with type II diabetes (n ¼ 20). MEASUREMENTS: All subjects had a normal fasting plasma glucose and glucose tolerance. Blood was collected for the determination of plasma insulin, adiponectin, triglyceride, and free fatty acids. Body composition was assessed with dual-energy X-ray absorptiometry and whole-body insulin sensitivity with a euglycaemic, hyperinsulinaemic clamp. Postprandial response over 6 h was determined for plasma adiponectin, glucose, insulin, triglyceride, and free fatty acids. Adiponectin was measured by commercial RIA and its polypeptide structure examined by Western blotting. RESULTS: The relatives were more insulin resistant and had increased adiposity compared with control subjects. There was no significant difference in postprandial response in fatty acids, triglyceride, or insulin between the groups. Postprandial levels of adiponectin measured by radioimmunoassay were not significantly different from fasting levels, and no breakdown products of adiponectin were detectable in postprandial samples by Western blotting. CONCLUSIONS: Levels of circulating adiponectin do not alter in response to a fat meal, despite evidence in mice that acute changes in adiponectin significantly affect postprandial fatty acid flux. Moreover, a fat meal challenge did not lead to significant activation of adiponectin by proteolytic conversion.

Acute Effects of Dietary Fat on Inflammatory Markers and Gene Expression in First-Degree Relatives of Type 2 Diabetes Patients

“…Moreover, we found no effect of either test meal on plasma adiponectin. This agrees with some previous studies on the impact of fat on plasma adiponectin in insulin-sensitive and insulin-resistant individuals [36]. Whereas, in the majority of studies, plasma adiponectin decreased in response to a high-fat meal [10,11].…”

The metabolism of isoforms of human adiponectin: studies in human subjects and in experimental animals

“…Postprandial values of triglyceride, insulin, non-esterified fatty acid and triglyceride were similar in the relatives of patients with diabetes and control subjects, and to those in similar studies using the same fat meal (15,16). Glucose levels were essentially unchanged, and there was no significant difference (, 5%) between the proportions of each adiponectin isomer present in basal and postprandial samples.…”

“…The protocols used to characterise the subjects and administer a fat meal and an oral glucose tolerance test have been reported previously in a study on a similar group of subjects (15,16). Body composition was assessed by dual energy emission x-ray absorptiometry (DEXA) and whole-body insulin sensitivity by a 120-min euglycaemic, hyperinsulinaemic clamp.…”

Adipokines in NASH: Postprandial Lipid Metabolism as a Link Between Adiponectin and Liver Disease *

“…Peake et al 26 found no difference in adiponectin response to a mixed meal between normal and insulinresistant subjects over a 6-hour period; however, basal adiponectin values were similar in the two groups, and the mixed meal elicited a significant insulin rise. 26 Vuppalanchi et al 27 found no difference in adiponectin response to a mixed meal between NASH patients and controls after 3 hours. It is possible that the abundance of adiponectin in blood, as compared with any other adipokines, and its long half-life (2.5-6 hours) may have masked any acute regulatory action of lipid load over the short term in previous studies.…”

“…The absence of carbohydrate in the test meal was designed to prevent the significant postprandial glucose and insulin increase elicited by mixed meals used in other studies. [26][27][28] The ability of insulin to suppress human adiponectin gene expression 29 and the release of FFA and to enhance triglyceride catabolism may in fact affect postprandial lipid and adiponectin responses. 30 The higher postprandial lipid response observed in our patients could play a role in liver Tg accumulation, as the magnitude of FFA increase correlated significantly with the severity of hepatic steatosis.…”